ArticleOncogene2004
Enhanced tenascin-C expression and matrix deposition during Ras/TGF-beta-induced progression of mammary tumor cells.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 48 citations in OpenAlex.
- RAS-mediated tumor stress adaptation and the targeting opportunities it presents.Disease models & mechanisms · 2022Article
- Review
- Collection on reports of molecules linked to epithelial-mesenchymal transition in the process of treating metastasizing cancer: a narrative review.Annals of translational medicine · 2021Review
- Lotus leaf extract inhibits ERNutrition & metabolism · 2021Article
- Latent TGF-β Activation Is a Hallmark of the Tenascin Family.Frontiers in immunology · 2021Article
- Novel Human Tenascin-C Function-Blocking Camel Single Domain Nanobodies.Frontiers in immunology · 2021Article
- Castration-induced stromal remodeling disrupts the reconstituted prostate epithelial structure.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Mechanochemical Signaling of the Extracellular Matrix in Epithelial-Mesenchymal Transition.Frontiers in cell and developmental biology · 2019Review
- Forcing through Tumor Metastasis: The Interplay between Tissue Rigidity and Epithelial-Mesenchymal Transition.Trends in cell biology · 2016Review
- Tenascin-C Signaling in melanoma.Cell adhesion & migration · 2015Review
- The motile breast cancer phenotype roles of proteoglycans/glycosaminoglycans.BioMed research international · 2014Review
- Extracellular matrix macromolecules: potential tools and targets in cancer gene therapy.Molecular and cellular therapies · 2014Review
- Expression of hypoxia-inducible factor 1 alpha in papillary thyroid carcinoma is associated with desmoplastic stromal reaction and lymph node metastasis.Virchows Archiv : an international journal of pathology · 2013Article
- Article
- How do tenascins influence the birth and life of a malignant cell?Journal of cellular and molecular medicine · 2012Review
- Defining the origins of Ras/p53-mediated squamous cell carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Tenascins and the importance of adhesion modulation.Cold Spring Harbor perspectives in biology · 2011Review
- Tenascin C induces epithelial-mesenchymal transition-like change accompanied by SRC activation and focal adhesion kinase phosphorylation in human breast cancer cells.The American journal of pathology · 2011Article
- Annexin A1 attenuates EMT and metastatic potential in breast cancer.EMBO molecular medicine · 2010Article
- The activation of Proteinase-Activated Receptor-1 (PAR1) mediates gastric cancer cell proliferation and invasion.BMC cancer · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression of tenascin-C (TN-C) in breast carcinomas has been associated with a migratory or even invasive tumor cell phenotype. The mechanisms regulating expression and matrix deposition of TN-C in normal and cancerous breast tissues are, however, little understood. Here, we demonstrate that mouse mammary epithelial cells (EpH4) transformed by oncogenic Ha-Ras (EpRas) overexpress TN-C, which accumulates in the cytoplasm. When EpRas cells undergo epithelial-mesenchymal transition (EMT) in response to TGFbeta1, they secrete TN-C into the culture medium. In EpRas cells undergoing TGFbeta1-induced EMT in three-dimensional (3D)-collagen gel cultures, TN-C was deposited into an extracellular matrix (ECM) already containing fibronectin and perlecan. Under less physiological 2D plastic cultures, EpRas cells undergoing EMT failed to deposit TN-C into an (apparently incomplete) ECM. Ras-downstream signaling was dissected by pharmacological inhibitors and effector-specific Ras mutants (V12S35, V12C40), specifically inhibiting or activating ERK/MAPK or PI3K signaling, respectively. We showed that TN-C overexpression required a hyperactive ERK/MAPK-signaling pathway, while elevated PI3K signaling did not enhance TN-C expression. Similarly, tumors induced by cells exhibiting hyperactive ERK/MAPK signaling showed expression of TN-C in the tumor cells themselves, while only endothelial cells expressed TN-C in tumors caused by the V12C40 mutant (incapable of EMT in vivo). Taken together, our data indicate that hyperactive ERK/MAPK signaling causes enhanced expression of TN-C, while its secretion is induced by TGFbeta1 and both signals cooperate in TN-C matrix deposition. Importantly, both signals also cooperate to induce EMT in vitro and tumor progression/metastasis in vivo.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.